Basic and Biobehavioral Research: About Biological Mechanisms of Psychosocial Effects on Disease (BiMPED)

The objective of the BiMPED initiative is to elucidate biological and molecular mechanisms associated with biobehavioral influences on cancer progression.

Managed by the Basic and Biobehavioral Research Branch, BiMPED encourages mechanistic studies to identify biological signaling pathways that might inform how behavioral stress and other influences on tumorigenesis are mediated by the central nervous system.

Our intent is to evaluate and encourage research that explores how neurotransmitters and neuropeptides associated with biobehavioral factors influence tumor processes like angiogenesis, apoptosis, invasion, inflammation, and metastasis.

This initiative encourages transdisciplinary research that bridges basic cancer biology and biobehavioral science to advance our fundamental knowledge of the extent and specificity by which central nervous system-regulated factors like stress, chronic depression, and social support might regulate tumor biology.

Research Agenda

The Basic and Biobehavioral Research Branch supports research in cancer prevention and control supporting research in these areas:

How broad are the influences of the physiologic stress response on tumor biology?

Which tumor types (and tumor genomes) are sensitive?

At which phase of disease are these effects most pronounced (initiation, regression, progression, and/or relapse; during the perioperative period or following surgery?

What types of biobehavioral factors cause physiological stress responses that are most influential for a given tumor type or stage (e.g., stress, depression, social support, optimism)?

The responses to stressors involve central nervous system (CNS) perceptions of threat and subsequent activation of the autonomic nervous system (ANS) and the hypothalamic–pituitary–adrenal (HPA) axis. Catecholamines, glucocorticoids and other stress hormones are subsequently released from the adrenal gland, brain and sympathetic nerve terminals and can modulate the activity of multiple components of the tumour microenvironment. Effects include the promotion of tumour-cell growth, migration and invasive capacity, and stimulation of angiogenesis by inducing production of pro-angiogenic cytokines. Stress hormones can also activate oncogenic viruses and alter several aspects of immune function, including antibody production, cytokine production profiles and cell trafficking (. Collectively, these downstream effects create a permissive environment for tumour initiation, growth and progression. CRF, corticotrophin-releasing factor; IL-6, interleukin-6; MMP, matrix metalloproteinase; VEGF, vascular endothelial growth factor.